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Is There a Link Between Autism and Glyphosate-Formulated Herbicides?

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Is There a Link Between Autism and Glyphosate-Formulated Herbicides? Journal of Autism ISSN 2054-992X | Volume 3 | Article 1 Review Open Access Is there a link between autism and glyphosate-formulated herbicides? James E. Beecham1 and Stephanie Seneff2* *Correspondence: [email protected] CrossMark ← Click for updates 1Consultant Pathologist (Retired) University of Florida, Gainesville, USA. 2MIT Computer Science and Artificial Intelligence Laboratory, Massachusetts Institute of Technology, USA. Abstract Glyphosate is the most widely used herbicide on the planet, and its increasing use over time in the United States aligns well with the increasing rates of autism determined by the Centers for Disease Control. Based on the known mechanism of glyphosate toxicity, we hypothesize that a pregnant woman’s exposure at mid- pregnancy to glyphosate-formulated herbicides (GFH) may produce, in her unborn child’s brain, anatomic alterations of cortical neuron layering remarkably similar to those found in the brains of humans with autism. Glyphosate’s known ability to chelate manganese ions combined with evidence of severely depleted serum manganese in cows exposed to glyphosate makes it likely that glyphosate would induce manganese deficiency in humans, interfering with the function of manganese-dependent enzymes. In particular, this would affect the maternal pituitary’s manganese-dependent Protein Phosphatase 1 (PP1) enzyme, resulting in a significant reduction in maternal serum levels of Thyroid-Stimulating Hormone (TSH). A study of mid-pregnancy maternal TSH serum levels in human mothers has found a statistical correlation of reduced TSH to increased risk of autism in offspring. Since insufficient thyroid stimulation by TSH or by iodine deficiency would both induce hypothyroidism, effects of iodine deficiency can be expected to emulate effects of TSH deficiency. Cortical neuron disarrangements have been produced in the brains of offspring of rat dams fed an iodine-deficient diet, and such foci of disordered cortical neurons are characteristically found in human autistic brains. While the research literature on glyphosate’s endocrine disrupting effects is limited, diverse evidence from animal studies reveals effects that suggest impaired thyroid function. If our hypothesis can be substantiated by a focused research effort, it would provide further justification for reducing or, ideally, eliminating glyphosate-formulated herbicide exposures in pregnant women. Keywords: Autism, glyphosate, manganese, hypothyroidism, topoisomerase, protein phosphatase, herbicide, neurodevelopment Introduction that the only pesticide whose usage rates have gone up dra- The prevalence of autism has been rising at an alarming rate matically exactly in step with the rise in autism is glyphosate, in the United States over the past two decades, as determined and it is the most used herbicide on the planet. Pesticides are for example by the progressive rise in the number of children clearly toxic as that is their intent, and a strong correlation in in the public school system designated as autistic under the the rise of a serious disorder with a toxic chemical can not be Individuals with Disabilities Education act (IDEA). The pattern simply dismissed. of this rise is extremely well matched temporally to the rising An initiative undertaken by the organization, Moms Across use of glyphosate on corn and soy crops, as pointed out in America, has found levels of glyphosate in breast milk ranging an article by Swanson et al., and illustrated in their figure 23, from 76 mg/l to 166 mg/l in 3 out of 10 test samples (see: http:// reproduced here as Figure 1 [1]. The data plotted in this figure www.momsacrossamerica.com/ glyphosate testing results). are readily available from U.S. government sources on the Web, A European study of glyphosate residues in urine of humans and the correlation is nearly perfect (0.99) (p<1.1E-6). While and animals found significantly more glyphosate in the urine correlation does not necessarily mean causation, it is striking of humans eating a conventional diet compared to those eat- © 2016 Seneff et al; licensee Herbert Publications Ltd. This is an Open Access article distributed under the terms of Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0). This permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Beecham et al. Journal of Autism 2016, http://www.hoajonline.com/journals/pdf/2054-992X-3-1.pdf doi: 10.7243/2054-992X-3-1 Autistic brains, during fetal development, appear to experience a disorder of neuron migration, at least in small foci. Stoner et al., found that autistic brains have small scattered foci of abnormal neocortex in which the usual 6 layers of neurons are instead blurred and ill-defined [4]. In addition to disorder in arrangement, some neurons in autism remained scattered within the white matter, apparently unable to migrate properly through the white matter and into the gray matter (Figure 3) as would normally occur. Neurons within these disordered foci in autistic brains also have a reduced content of calcium- buffering molecules, as demonstrated by reduced CALB1 in-situ hybridization staining. Lopez-Hurtado et al., found autistic brains to have a focal reduction in number of neurons and a focal increase in number of glial cells in areas related to speech processing [5]. Figure 1. Trends over time in the number of children with autism according to the IDEA and in the use of glyphosate on corn and soy crops. These data are readily available from the U.S. government from Web-based resources. Figure reproduced with permission from Swanson et al. [73]. ing an organic diet (P<0.0001) [2]. Furthermore, humans with chronic diseases had higher levels than those who were healthy. In this paper, we develop the hypothesis that glyphosate’s potential link to autism can be explained in part through an adverse effect on the thyroid gland of both the mother and the child during gestation. In the developing human brain, in order to form proper neuronal circuits and cortical architecture, neurons must migrate and assemble in an organized manner. Figure 3. Schematic of neocortex neuron arrangement, normal Under normal circumstances, immature neurons migrate (left) versus focus of abnormal cortex in autistic brain (right). through the paraventricular white matter to assemble in the Note the autistic brain has small foci with excess neurons, a neocortex and progressively form, within the gray matter, a blurring of layering, and numerous neurons still remaining distinct 6 layered pattern of neurons [3] (see Figure 2). within the white matter. Figure 2. (Modified from Grieg et al. [3]) The 6 layered pattern of neocortical neurons. In humans, this pattern forms during in-utero fetal development during weeks 12 to 20. In the uppermost layer, the CajalRetzius cells (shown in orange) produce reelin, a protein which assists in properly arranging the migrating neurons. Definitions: VZ: Ventricular zone; SVZ: Subventricular zone; SP: Subplate. 2 Beecham et al. Journal of Autism 2016, http://www.hoajonline.com/journals/pdf/2054-992X-3-1.pdf doi: 10.7243/2054-992X-3-1 During neurodevelopment in children with autism, there is an Review excess of focal neurons in the early stages as compared to the Autism is a complex disorder of brain development charac- same age in typical fetal/childhood development, up to 70% terized by repetitive behavior patterns and difficulties with more neurons in foci early on in autistic brains as compared social communication and interaction. It is believed to usually to normal neurodevelopment. In the neocortex, these extra originate in utero, although there is also a form of regressive neurons migrate improperly, forming blurred indistinct layer- autism that occurs postnatally, which is not the subject of ing, with many neurons remaining within the white matter. this paper. Maternal hypothyroidism is linked to autism in Stoner et al., found such a pattern in 10 of the 11 autistics the fetus [9,10] and there is evidence from the neurological they studied, and also in one control brain, of a child who research literature supporting this link. We begin here with had suffered seizures [4]. Many of these excess disordered a review of selected features regarding the normal thyroid- neurons proceed through apoptosis at a later stage, and related physiology relevant to our theory. As is well-known, this programmed cellular death appears to stimulate local the in-utero fetus is heavily dependent upon the mother’s gliosis/glial activation. production of thyroid hormone for neurodevelopment (see In a previous article on autism [6], we presented evidence Figure 4). Maternal T4 (thyroxine) and T3 (triiodothyronine) supporting our theory that glyphosate may play a causal role cross the placenta and interact with cells in the fetus [11]. in autism through its mimicry of the amino acid glycine. We analyzed data suggesting that glyphosate’s mimicry would disrupt calcium inflow to immature neurons. For example, glyphosate may act at the glycine receptor of neurons (GlyR) which is a key to modulating the amount of chloride outflow from the immature neuron. This could cause inappropriate neuron membrane depolarizations, which then could force haphazard dislodgements of the magnesium ion from its blocking position within the N-methyl-D-aspartate (NMDA) receptor channel at the neuron membrane. This magnesium ion dislodgment could lead to excess and haphazard inflows of cal- cium into the immature neuron (if simultaneously the glycine binding site and glutamate binding site of the NMDA receptor are also agonistically bound). Glyphosate would plausibly induce excess bioavailability of glutamate by interfering with manganese-dependent conversion of glutamate to glutamine. One signal that such excess calcium inflows are happening to neurons in autistic brains would be the finding of a reduc- tion in the calcium buffering capacity remaining in neurons. Stoner et al., demonstrated just such a reduced calcium buffer content within poorly migrating autistic neurons [4]. The inter- ested reader is referred to our previous paper for more details.
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